Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose

Detalhes bibliográficos
Autor(a) principal: Perdigoto, Rui
Data de Publicação: 2003
Outros Autores: Furtado, Alexandre L., Porto, Armando, Rodrigues, Tiago B., Geraldes, Carlos F. G. C., Jones, John G.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10316/4810
https://doi.org/10.1016/S0925-4439(03)00018-8
Resumo: Plasma glucose 2H enrichment was quantified by 2H NMR in patients with cirrhosis (n=6) and healthy subjects (n=5) fasted for 16 h and given 2H2O to ~0.5% body water. The percent contribution of glycogenolysis and gluconeogenesis to glucose production (GP) was estimated from the relative enrichments of hydrogen 5 and hydrogen 2 of plasma glucose. Fasting plasma glucose levels were normal in both groups (87±7 and 87±24 mg/dl for healthy and cirrhotic subjects, respectively). The percent contribution of glycogen to GP was smaller in cirrhotics than controls (22±7% versus 46±4%, P<0.001), while the contribution from gluconeogenesis was larger (78±7% versus 54±4%, P<0.001). In all subjects, glucose 6R and 6S hydrogens had similar enrichments, consistent with extensive exchange of 2H between body water and the hydrogens of gluconeogenic oxaloacetate (OAA). The difference in 2H-enrichment between hydrogen 5 and hydrogen 6S was significantly larger in cirrhotics, suggesting that the fractional contribution of glycerol to the glyceraldehyde-3-phosphate (G3P)-moiety of plasma glucose was higher compared to controls (19±6% versus 7±6%, P<0.01). In all subjects, hydrogens 4 and 5 of glucose had identical enrichments while hydrogen 3 enrichments were systematically lower. This reflects incomplete exchange between the hydrogen of water and that of 1-R-dihydroxyacetone phosphate (DHAP) or incomplete exchange of DHAP and G3P pools via triose phosphate isomerase.
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spelling Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucoseGlucoseDeuteriumGlycogenolysisCirrhosisPlasma glucose 2H enrichment was quantified by 2H NMR in patients with cirrhosis (n=6) and healthy subjects (n=5) fasted for 16 h and given 2H2O to ~0.5% body water. The percent contribution of glycogenolysis and gluconeogenesis to glucose production (GP) was estimated from the relative enrichments of hydrogen 5 and hydrogen 2 of plasma glucose. Fasting plasma glucose levels were normal in both groups (87±7 and 87±24 mg/dl for healthy and cirrhotic subjects, respectively). The percent contribution of glycogen to GP was smaller in cirrhotics than controls (22±7% versus 46±4%, P<0.001), while the contribution from gluconeogenesis was larger (78±7% versus 54±4%, P<0.001). In all subjects, glucose 6R and 6S hydrogens had similar enrichments, consistent with extensive exchange of 2H between body water and the hydrogens of gluconeogenic oxaloacetate (OAA). The difference in 2H-enrichment between hydrogen 5 and hydrogen 6S was significantly larger in cirrhotics, suggesting that the fractional contribution of glycerol to the glyceraldehyde-3-phosphate (G3P)-moiety of plasma glucose was higher compared to controls (19±6% versus 7±6%, P<0.01). In all subjects, hydrogens 4 and 5 of glucose had identical enrichments while hydrogen 3 enrichments were systematically lower. This reflects incomplete exchange between the hydrogen of water and that of 1-R-dihydroxyacetone phosphate (DHAP) or incomplete exchange of DHAP and G3P pools via triose phosphate isomerase.http://www.sciencedirect.com/science/article/B6T1Y-480C3H1-1/1/e724e4a4e606c2aabcfd804b0759b2bf2003info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleaplication/PDFhttp://hdl.handle.net/10316/4810http://hdl.handle.net/10316/4810https://doi.org/10.1016/S0925-4439(03)00018-8engBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1637:2 (2003) 156-163Perdigoto, RuiFurtado, Alexandre L.Porto, ArmandoRodrigues, Tiago B.Geraldes, Carlos F. G. C.Jones, John G.info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2021-08-31T07:37:56Zoai:estudogeral.uc.pt:10316/4810Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:43:28.265780Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
title Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
spellingShingle Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
Perdigoto, Rui
Glucose
Deuterium
Glycogenolysis
Cirrhosis
title_short Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
title_full Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
title_fullStr Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
title_full_unstemmed Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
title_sort Sources of glucose production in cirrhosis by 2H2O ingestion and 2H NMR analysis of plasma glucose
author Perdigoto, Rui
author_facet Perdigoto, Rui
Furtado, Alexandre L.
Porto, Armando
Rodrigues, Tiago B.
Geraldes, Carlos F. G. C.
Jones, John G.
author_role author
author2 Furtado, Alexandre L.
Porto, Armando
Rodrigues, Tiago B.
Geraldes, Carlos F. G. C.
Jones, John G.
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Perdigoto, Rui
Furtado, Alexandre L.
Porto, Armando
Rodrigues, Tiago B.
Geraldes, Carlos F. G. C.
Jones, John G.
dc.subject.por.fl_str_mv Glucose
Deuterium
Glycogenolysis
Cirrhosis
topic Glucose
Deuterium
Glycogenolysis
Cirrhosis
description Plasma glucose 2H enrichment was quantified by 2H NMR in patients with cirrhosis (n=6) and healthy subjects (n=5) fasted for 16 h and given 2H2O to ~0.5% body water. The percent contribution of glycogenolysis and gluconeogenesis to glucose production (GP) was estimated from the relative enrichments of hydrogen 5 and hydrogen 2 of plasma glucose. Fasting plasma glucose levels were normal in both groups (87±7 and 87±24 mg/dl for healthy and cirrhotic subjects, respectively). The percent contribution of glycogen to GP was smaller in cirrhotics than controls (22±7% versus 46±4%, P<0.001), while the contribution from gluconeogenesis was larger (78±7% versus 54±4%, P<0.001). In all subjects, glucose 6R and 6S hydrogens had similar enrichments, consistent with extensive exchange of 2H between body water and the hydrogens of gluconeogenic oxaloacetate (OAA). The difference in 2H-enrichment between hydrogen 5 and hydrogen 6S was significantly larger in cirrhotics, suggesting that the fractional contribution of glycerol to the glyceraldehyde-3-phosphate (G3P)-moiety of plasma glucose was higher compared to controls (19±6% versus 7±6%, P<0.01). In all subjects, hydrogens 4 and 5 of glucose had identical enrichments while hydrogen 3 enrichments were systematically lower. This reflects incomplete exchange between the hydrogen of water and that of 1-R-dihydroxyacetone phosphate (DHAP) or incomplete exchange of DHAP and G3P pools via triose phosphate isomerase.
publishDate 2003
dc.date.none.fl_str_mv 2003
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://hdl.handle.net/10316/4810
http://hdl.handle.net/10316/4810
https://doi.org/10.1016/S0925-4439(03)00018-8
url http://hdl.handle.net/10316/4810
https://doi.org/10.1016/S0925-4439(03)00018-8
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1637:2 (2003) 156-163
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